ArticleOncology letters2014
GSTM3 reverses the resistance of hepatoma cells to radiation by regulating the expression of cell cycle/apoptosis-related molecules.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Investigating the Mechanisms of 15-PGDH Inhibitor SW033291 in Improving Type 2 Diabetes Mellitus: Insights from Metabolomics and Transcriptomics.Metabolites · 2024Article
- GSTM3 enhances radiosensitivity of nasopharyngeal carcinoma by promoting radiation-induced ferroptosis through USP14/FASN axis and GPX4.British journal of cancer · 2024Article
- Advancements in understanding mechanisms of hepatocellular carcinoma radiosensitivity: A comprehensive review.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2023Article
- Study of the dual biological impacts of aqueous extracts of normal and gamma-irradiatedJournal of Taibah University Medical Sciences · 2022Article
- Incorporation of DNA methylation into eQTL mapping in African Americans.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2021Article
- GSTM3 Function and Polymorphism in Cancer: Emerging but Promising.Cancer management and research · 2020Review
- Glutathione S-Transferase Mu-3 Predicts a Better Prognosis and Inhibits Malignant Behavior and Glycolysis in Pancreatic Cancer.Frontiers in oncology · 2020Article
- Effect of nine diets on mRNAs of phase-II conjugation enzymes in livers of mice.Xenobiotica; the fate of foreign compounds in biological systems · 2017Article
- Circulating Long Noncoding RNA UCA1 as a Novel Biomarker of Acute Myocardial Infarction.BioMed research international · 2016Article
- Gene expression analysis of pig cumulus-oocyte complexes stimulated in vitro with follicle stimulating hormone or epidermal growth factor-like peptides.Reproductive biology and endocrinology : RB&E · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiotherapy (RT) is a major modality of hepatoma treatment. However, liver tumors often acquire radioresistance, which contributes to RT failure. The exact mechanisms of the radioresistance in hepatoma cells are largely unknown. Glutathione S-transferase M3 (GSTM3) is a phase II transferase, however, recent studies have suggested that GSTM3 is a potential tumor suppressor. The purpose of the present study was to investigate the role of GSTM3 in reversing radioresistance, and to explore the molecular mechanism of this in the human radiation-resistant PRF/PLC/5R hepatocellular carcinoma (HCC) cell line. The radioresistant PLC/PRF/5R cells were used as cell model, and were derived from PLC/PRF/5 parental cells using fractionated irradiation. The radiosensitivity of the cells was tested by clonogenic assay and flow cytometry analyses. The expression of B-cell chronic lymphocytic leukemia/lymphoma 2 (Bcl-2), Bax, p21, p27 and p53 was analyzed by quantitative polymerase chain reaction and immunoblotting with or without radiation. The results showed that the expression levels of GSTM3 were significantly lower in the PLC/PRF/5R cells than in the PLC/PRF/5 parental cells. GSTM3 overexpression sensitized the PLC/PRF/5R cells to radiation mainly though induction of apoptosis. According to the evidence from Annexin-V/PI staining, it markedly increased the percentage of apoptotic PRF/PLC/5R cells. The clonogenic assay indicated that GSTM3 significantly decreased the RT survival fraction in PRF/PLC/5R cells. Furthermore, GSTM3 increased the expression of cell cycle- and apoptosis-related genes (Bcl-2, Bax, p21, p27 and p53) in PRF/PLC/5R cells with irradiation. These findings suggest that GSTM3 plays an pivotal role in reversing the radioresistance of HCC and may be a potential target for sensitizing HCC cells to RT. The underlying mechanisms may be linked to the cell cycle arrest and apoptosis facilitation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.